PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14613873-7	2003	RESULTS: PAR2-AP (10(-7)-3 x 10(-5) M) caused an endothelium-dependent relaxation abolished by N(omega)-nitro-L-arginine methyl ester, L-NAME, and by the guanylyl cyclase inhibitor, 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), but unaffected by geldanamycin.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	230-233	F2R like trypsin receptor 1	Rattus norvegicus	9-13	
9660401-11	1998	Furthermore, in another group ODQ (10(-5) mol/L) inhibited responses to SLIGRL to a degree similar to that seen with L-NNA, consistent with a mechanism of PAR-2-mediated vasodilatation that involves activation of guanylate cyclase by nitric oxide.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	30-33	F2R like trypsin receptor 1	Rattus norvegicus	155-160	
24576493-5	2014	Vasodilation induced by the PAR2 agonist SLIGRL in arteries from control-diet rats was abolished by L-NAME/ODQ, but unaffected by IBTX.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	107-110	F2R like trypsin receptor 1	Rattus norvegicus	28-32